Intrauterine growth restriction (IUGR) is a major cause of perinatal morbidity and mortality. Because nitric oxide (NO) has been implicated in IUGR and the insulin-like growth factor (IGF) axis is essential for fetal growth, our goal was to determine if chronic administration of a NO inhibitor could induce IUGR, and if disruption of the IGF axis was associated with these findings. Six gravid macaques were chronically administered NG-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg/day) via Alzetb osmotic minipumps during the late second and third trimesters. Maternal blood pressure, complete blood couts (CBCs), indirect measures of NO levels, and urinalyses were evaluated periodically during the treatment period. Each week, fetal growth was assessed sonographically. Roughly every 10 days until tissue harvest (GD 145), fetal blood samples were collected with ultrasound guidance for CBCs; studies of circulating IGF-I, IGF-II, IGF binding proteins; and nitrite/nitrate levels as stable oxidation products of NO synthesis. All evaluations of the dam were unremarkable and there was no evidence of maternal compromise during the study. A significant effect on fetal growth was observed and assessments of fetal sera showed reduced curculating IGF-I whereas IGF binding protein (IGFBP-3) was substantially elevated. Fetal and maternal NO production was not changed with treatment. These studies show that chronic maternal L-NAME administration (1) results in significant IUGR with selective tissue loss in the presence of brain sparing; (2) disrupts the fetal IGF-I:IGFBP-3 ratio; (3) does not result in a reduction in fetal or maternal circulating nitrate/nitrite levels; and (4) does not alter maternal blood pressure or other clinical parameters. Therefore, administration of the NO synthase inhibitor, L-NAME, provides a means for modelling mechanisms of fetal growth restriction without compromised maternal health. *KEY*Sonography, Fetus, Growth restriction, IGF, Nitric oxide